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Uremic Syndrome

Acute Kidney Injury
Chronic Kidney Disease

Lecture 3: Genito-urinary system.
10 – 08 – 2009.

Uremic Syndrome
Acute Kidney Injury
Chronic Kidney Disease

nephron
the functional unit of the kidney
•capable of forming urine
•has two major components:
glomerulus
tubule:

proximal
loop of Henle
distal
collecting

Interstitium

structural organization
renal parenchyma
cortex
medulla

nephrons

cortical
juxtamedullary

Renal Function:
Excretory
Regulatory
Endocrine
Excretory Function:
Glomerular
Glomerular Filtration Rate (GFR)
Creatinin Clearance.
UxV/P ml/min

GFR:
inulin clearance
EDTA isotop
99 Tc
isotop
Iohexal High Performance
liquid chromatography

Clinical setting:
eGFR: Cockroft-Gault Formula
MDRD Formula

Cockroft-Gault Formula
Male:

Or

Female:

Or

1,23 x (140 – age ) x BW (kg)
Ccr = ----------------------------------------- ml/min
Scr (µ mol/min)
140 – age (yrs) x BW (kg)
Ccr = ----------------------------------------- ml/min
72x Scr (mg/dl)
140 – age (yrs) x BW (kg)
Ccr = ----------------------------------------- ml/min
70 x Scr (mg/dl)
Ccr( male) x o.85.

NKF-KDOQI recommendation
Adults
Cockcroft-Gault equation:
GFR (ml/min) = (140-age) X Weight /72 x Scr X(0.85 if female)
MDRD (modification of diet in renal disease) equation:
GFR (ml/min/1.73 m2) = 186 X (SCr) -1.154 X (Age) -0.203 X
(0.742 if female) X (1.210 if black)

Children
Schwartz equation: GFR (ml/min) = 0.55 x length/Scr
Counahan-Barratt equation: GFR (ml/min/1.73m 2)= 0.43 X Length/Scr

Renal Function:
Excretory
Regulatory
Endocrine
Regulatory Function:
Tubulo-interstitial
* water and electrolyte balance
* acid-base balance

Renal Function:
Excretory
Regulatory
Endocrine
Endocrine Function:
renal parenchymal
renin, prostaglandin,
erythropoietin, calcitriol

Uremic Toxicity

Uremia-1
 Greek

words : urine + blood = uremia
 Uremia is the retention of excessive by
products of protein metabolism in the blood
and the toxic condition produced thereby.

Uremia-2
 Uremia

is a toxic syndrome caused by severe
glomerular insufficiency, associated with
disturbances in tubular and endocrine functions of
the kidney.
 It is characterized by retention of toxic
metabolites, associated with changes in volume
and electrolyte composition of the body fluids and
excess or deficiency of various hormones (uremic
syndrome).

Toxic effects of uremic plasma

variety disturbances:
anemia, immunologic deficiency,
bleeding tendency, disorders of
carbohydrate and lipid metabolism,
and various membrane transport
disturbances.

Uremia
An excess in the blood of urea, creatinine and other
nitrogenous end products with signs and symptoms listed .
 General
– Fatigue, weakness
– Pruritus

 Mental/neurologic

status change

– Uremic encephalopathy
– Seizures
– Asterixis

 GI

disturbance

– Anorexia, early satiety, N/V,

 Uremic Pericarditis
 Platelet

dysfunction/bleeding

Uremic toxins
Small, middle-sized, and large molecules
 Size:

Small : < 500 ( or 350 ) Da
Middle : 500 ~ 5,000 Da
Large : > 5,000 Da

Toxicity of inorganic substances
in uremia
 Water
 Sodium
 Potassium
 Hydrogen

ions
 Magnesium
 Phosphate
 Sulfate
 Trace elements

Organic compounds of Low
molecular weight
 Urea
 Creatinine
 Guanidines

(other than creatinine)
 Methylguanidine
 Guanidinosuccinic Acid (GSA)
 Methylated Arginine Metabolites
 Other guanidines
 Products of Nucleic Acid Metabolism

Organic compounds of Low molecular weight

Urea (1)
 The

most important end product of nitrogen
metabolism in mammals and account for
85% of the urinary nitrogen excretion.
 Blood concentration: glomerular filtration
rate, nitrogen intake, balance between
endogenous protein synthesis and
breakdown.

Organic compounds of Low molecular weight

Urea(3)
 High

concentration: headache, fatigue,
nausea, vomiting, glucose intolerance, and
bleeding.
 The most severe uremic GI, CV, mental and
neurologic changes were not seen.
 Considered “mild” uremic toxin .
 Role in the pathophysiology of uremia is not
well defined.

Serum Creatinine
 Serum

creatinine is a reflection of creatinine
clearance
 Creatinine production is determined by muscle mass
and must be interpreted with respect to pt’s age,
weight and sex.
 Creatinine is filtered and secreted and tends to over
estimate GFR.
 Certain diseases and medications interfere with
correlation between serum Cr and GFR. (i.e.. Acute
glomerulonephritis, trimethoprim, cimetidine)

Serum Creatinine (cont.)
 None

of the equations accurately determine
GFR in ARF. (Assume Cr is stable)
 More accurate techniques involve nuclear
medicine studies and GFR scans.
 New biochemical markers investigated (i.e..
Cystatin C)

Organic compounds of Low molecular weight

Other guanidines
 The

concentrations of various guanidine
compounds are higher in uremic patients.
 Some toxic in vitro effects seem to have been
obtained at concentrations similar to those in
uremic body fluids.
 Most in vitro and in vivo toxic effects have been
observed at much higher concentrations than are
found in uremic patients
 The role of guanidines as uremic toxins is still not
well defined.

Product of Nucleic Acid
Metabolism










Uric acid and other purine derivatives
Cyclic AMP
Pyridine derivatives
Amino acids, dipeptides, and tripeptides
Sulfur amino acids
Aliphatic amines
Aromatic amines
Polyamines
Indoles
Phenols
Carbonhyrate derivatives

Middle molecules as uremic
toxins
The middle molecule hypothesis:
 Peritoneal

membrane was more leaky and thus
more effective at removing middle molecules than
the hemodialysis membranes.
 It is well established that CAPD patients may
survive and thrive as well as HD patients do, even
though their average weekly clearance of urea is
considerably lower than that for HD patients.

Toxic effects of crude MM
fractions
 Inhibition

of proliferation of undifferentiated cell
lines and hematopoietic cell lines, depression of
several immmune function, increase hemolysis,
cardiotoxicity, inhibition of platelet aggregation,
inhibition of glucose utilization, inhibit protein
synthesis and amino acid transport, inhibition of
mitochondrial respiration
 Inhibit osteoclast mitogenesis
 Some enzyme activities are also inhibited

Parathyroid hormone
 Incresed

in uremic patients as consequence of
phosphate retention, decreasing ionized calcium
stimulate parathyroid glands to increase PTH
secretion
 PTH hypersecretiopn in uremic patients :
encephalopathy, neuropathy, dementia, bone
disease, soft tissue calcification, hypertension,
cardiomegaly, carbohydrate intolerance, anemia,
sextual dysfunction

High-molecular-weight peptides
and proteins
 Ribonuclease
 Granulocyte-inhibiting
 Complement

proteins

factors
 Beta2-Microglobulin and Dialysis-related
amyloidosis

Uremic Syndrome
Acute Kidney Injury
Chronic Kidney Disease

Lecture 3: Genito-urinary system.
10 – 08 – 2009.

acute kidney injury: definition
ARF is an abrupt decline in glomerular and
tubular function, resulting in the failure of the
kidneys to excrete nitrogenous waste products
and to maintain fluid and electrolyte
homeostasis.

Epidemiology
5

% of hospitalized patients dev. ARF.
 0.5% of these patients require dialysis.
 20% of critical care admissions dev. ARF.
 Hospital acquired ARF usually develops in
the setting of ICU secondary to multisystem
organ failure.

RIFLE Classification
2004 ADQI group classification
 Risk (R) -Increase Cr x1.5 or Decrease GFR x 25% or UO
<0.5 ml/kg/hr x 6hrs
 Injury (I)- Increase Cr x2.0 or Decrease GFR x 50% or UO
<0.5 ml/kg/hr x 12hrs
 Failure (F)- Increase Cr x3.0 or Decrease GFR x75% or
anuria x 12 hours
 Loss (L)- Persistent ARF, complete loss of kidney function
x 4 weeks (needing RRT)
 End Stage Kidney Disease (E)- Loss of kidney function x 3
months

The Second International Consensus Conference of
the Acute Dialysis Quality Initiative (ADQI) Group

AKI

PRE RENAL

RENAL

Loss of intra-vas. vol
Reduced cardiac-output
Periferal Vasodilatation
Increased reno-vasc resistence
Reduced intra-glomerular pressure
ACE-i

POST RENAL

ACUTE KIDNEY INJURY
Pre-renal
Loss of intra-vasc vol..
BLEEDING
POLYURIA, SALT-LOOSING GN
G-I TRACT FLUIG LOSS
PROFUSE SWEATING

Reduced cardiac-output
CHF
CARDIOGENIC SHOCK
PERICARDIAL/TAMPONADE
MASSIVE LUNG EMBOLI

TISSUE TAUMA ETC

Perifer Vasodilatation
SEPSIS
ANTI-HIPERTENSIVE DRUGS
ANAPHYLAXIS

Reduced intraglom. pressure

Increase reno-vasc.resistence
SURGERY
ANESTEYHICS
HEPATORENAL SYNDR
VASOCONSTRICT DRUGS

ACE-i

AKI

PRERENAL

RENAL

POST RENAL

BIG VESSELS
SMALL VESSELS
GLOMERULAR
INTERSTITIUM
TUBULAR

BIG VESSELS
STENOSIS A.RENALIS
DIS.
THROMBOSIS/EMBOLI
MICROANGIOPATHY

SMALL VESSELS
VASCULITIS, ATHEROEMBOLIC
THROMBOTIC

GLOMERULAR:
Ix deposit glom. Disease
nephritis
psgn, lupus nephritis, MPGN etc
NSAID,

RPGN
Goodpasture syndr
Non Ix deposit

INTERSTITIUM
Acute interstitial
AB, Diuretics,

allopurinol dll

Wegener’s granulomatosis, Polyarteriitis
nodosa, Idiop. Cresc.GN

TUBULAR:
Renal ischemia: shock, bleeding, trauma, gram (-) bacteria,

AKI

PRERENAL

RENAL

POST RENAL
Stone, Crystals
Prostate, Ureteric
Stricture bilateral or unilateral in single
functioning kidney

MEDICAL

SURGICAL

Causes of ARF in Hospitalized
Patients
45% ATN
 Ischemia, Nephrotoxins
21% Prerenal
 CHF, volume depletion, sepsis
10% Urinary obstruction
4% Glomerulonephritis or vasculitis
2% Acute Interstitial Nephritis
1% Atheroemboli
etc

Pre Renal Azotemia
 Impaired

renal blood flow as a result of true
intravascular depletion, decreased effective
circulating volume to the kidneys, or agents that
impair renal blood flow.
 Urine and blood studies are helpful in diagnosing
pre renal ARF.
 Hyaline casts can be seen (Not an abnormal
finding).
 Treat with fluid boluses or continuous IVF, monitor
urine output.

Post Obstructive Uropathy
 Occurs

if both urinary outflow tracts are obstructed or
outflow tract of solitary kidney is obstructed.
 Patients with SUDDEN ONSET of anuria are likely to
have post obstructive uropathy.
 Primary causes include BPH, prostate and cervical cancer,
stones, strictures and retroperitoneal fibrosis.
 Bladder catheterization and Renal U/S to assess
hydronephrosis.
 Can have obstruction w/o hydronephrosis on U/S
 Monitor for post obstructive diuresis, hemorrhagic cystitis?

Intrinsic Acute Kidney Injury
Tubular (ATN)
2. Interstitial (AIN)
3. Glomerular (Glomerulonephritis)
4. Vascular
1.

ATN
 Most

common cause of ARF in hospitalized patients
 Contrast and aminoglycosides most often associated with
nonischemic ATN.
 3 phases:
1) Initiation phase- Renal injury lasting
hours to days.
2) Maintenance phase- Lasts days to
weeks. GFR and
U.O at lowest.
3) Recovery Phase- Postacute tubular necrosis diuresis.
Can still exp. uremia and hypovolemia as tubular function
not completely restored.

Acute Interstitial Nephritis
70% Drug hypersensitivity
 30% Antibiotics: PCNs (Methicillin), Cephalosporins, Cipro
 Sulfa drugs
 NSAIDs
 Allopurinol...
15% Infection
 Strep, Legionella, CMV, other bact/viruses
8% Idiopathic
6% Autoimmune Dz (Sarcoid, Tubulointerstitial nephritis/Uveitis)

AIN from Drugs
Renal damage is NOT dose-dependent
May take wks after initial exposure to drug
 Up to 18 mos to get AIN from NSAIDS!
But only 3-5 d to develop AIN after second exposure to drug





Fever (27%)
Serum Eosinophilia (23%)
Maculopapular rash (15%)
Bland sediment or WBCs, sterile pyuria most commonly seen
WBC Casts are common
Urine eosinophils on Wright’s or Hansel’s Stain
- Also see urine eos in RPGN, renal atheroemboli...
Treatment is to remove offending agents. Most patients recover complete kidney
function w/I one year.

Nephritic Syndromes
Type 1: Anti-GBM dz (Anti GBM Ab positive)
Goodpasture’s Disease
Anti-GBM
Type 2: Immune complex (Low compliment, elevated ESR)
 IgA nephropathy (Normal Compliment levels)
 Postinfectious glomerulonephritis
 Lupus nephritis
 Mixed cryoglobulinemia
 MPGN
 IBE
Type 3: Pauci-immune (ANCA positive, assoc with vasculitis)
 Wegner’s Disease
 Microscopic Polyangitis
 Churg-Strauss

Nephritic Syndromes
 Fever
 Oliguria
 Hematuria
 Htn
 RBC

casts
 Proteinuria (1-2grams usually)
 Treatment varies based on underlying disease

Renal Atheroembolic Dx
1% of Cardiac caths: atheromatous debris scraped from the
aortic wall will embolize
– Retinal
– Cerebral
– Skin (Livedo Reticularis, Purple toes)
– Renal (ARF)
– Gut (Mesenteric ischemia)
 Cr will NOT improve with IVF
 Diagnosis of exclusion: will NOT show up on MRI or Renal
U/S; WILL show up on renal bx
 Tx: supportive

acute renal failure: prevention
 recognize

patients at risk (postoperative states, cardiac
surgery, septic shock)

 prevent

progression from prerenal to renal

 preserve

renal perfusion

– isovolemia, cardiac output, normal blood pressure
– avoid nephrotoxins (aminoglycosides, NSAIDS, amphotericin)

Treatment
 Reverse

underlying causes and correct fluid
and electrolyte balances
 Treatment is supportive.
 Drugs such as mannitol, loop diuretics,
dopamine and CCB successful in promoting
diuresis in animals but not in humans.
 Dialysis as needed (IHD vs. CRRT)

acute renal failure: management
 treat

the underlying diseases
 strictly monitor intake and output (weight, urine output,
insensible losses, IVF)
 monitor serum electrolytes
 adjust medication dosages according to GFR
 avoid highly nephrotoxic drugs

nutrition
 provide

adequate caloric intake
 limit protein intake to control increases in BUN
 minimize potassium and phosphorus intake
 Limit Na/fluid intake
If adequate caloric intake can not be achieved
due to fluid limitations, some form of dialysis
should be considered

acute renal failure: fluid therapy
If patient is fluid overloaded
fluid restriction (insensible water losses)
 attempt furosemide 1-2 mg/kg (not evidence-based)
 Renal replacement/support therapy (see later)

If patient is dehydrated:
restore intravascular volume first
 then treat as euvolemic (below)

If patient is euvolemic:

restrict to insensible losses (30-35 ml/100kcal/24 hours) +
other losses (urine, chest tubes, etc)

Daily fluid allowance:
ALLOWANCE = Volume Excreted + I W L
24 hrs
Volume Excreted : Urine, vomitus, diarhea,
drain, etc
I W L : 500 ml / 24 hrs  50 kg BW T 37 0C
↑ 15 %  increment of 1 0C
Monitor daily BW

sodium
 most

patients have dilutional hyponatremia which
should be treated with fluid restriction

 severe

hyponatremia (Na< 125 mEq/L) or
hypernatremia (Na> 150 mEq/L): dialysis or
hemofiltration

Treatment of Hyperkalemia
 Calcium

Gluconate
 Glucose and Insulin
 Sodium Bicarbonate
 Diuretics (Lasix)
 Cation-exchange resins (Kayexalate)
 Dialysis

Acute Indications for Dialysis
AIUEO
 Acidosis

(metabolic)
 Ingestion of drugs/Ischemia
 Uremic syndrome
 Electrolytes (hyperkalemia)
 Overload (fluid)

MANAGEMENT
AKI

RRT/SUPPORT

FLUID
DIET

INDIKASI :

DRUG
DIALYSIS

Severe uremic symptoms
Urea >200 mg%,Cr >8 mg%PERITONEAL
HEMO
K > 7 mg%
Pericarditis
HEMOFILTRATION
Severe Asidosis
CAVH (d), CVVH (d)
Pulmonary Oedema
SCUF (d), SLEDD

Mortality/Morbidity
 Mortality

rates range from 7-80% depending on
patient’s other co morbidities.
 This rate has remained unchanged since the advent
of dialysis because of increasing age and co
morbid conditions.
 Most common cause of death associated with ARF
are sepsis, cardiac failure and respiratory failure.
 Mortality rates are lower for nonoliguric
(>400ml/day) then oliguric ARF (<400 ml/day).

Take Home Points
 Features of the history and physical examination

in addition to relevant lab and radiologic
investigations help to determine the most likely
cause(s) of ARF in a given patient

Take Home Points
 Management of a patient with ARF involves:
– Treating potentially life-threatening complications
– Reversing pre-renal and post-renal causes
– Minimizing further hemodynamic and toxic insults to

the kidney
– Admission and appropriate consultation
– Lack of evidence for converting oliguric to nonoliguric ARF

Uremic Syndrome
Acute Kidney Injury
Chronic Kidney Disease

CKD
PARENCHYMAL

OBSTRUCTIVE

GN
urolithiasis
Diabetic Nephropathy
Prostate
Nephrosclerotic/hypertension Ureteric Stricture
Policystic
Lupus
TBC

Definition of
Chronic Kidney Disease

AJKD 2002: 39(2)

NKF-KDOQI recommendation
Adults
MDRD (modification of diet in renal disease) equation:
GFR (ml/min/1.73 m2) = 186 X (SCr) -1.154 X (Age) -0.203 X
(0.742 if female) X (1.210 if black)

Children
Schwartz equation: GFR (ml/min) = 0.55 x length/Scr
Counahan-Barratt equation: GFR (ml/min/1.73m 2)= 0.43 X
Length/Scr

Pivotal Rote of Glomerular Hypertension
in the Initiation and Progression
of Structural Injury.
Systemic
Hypertension

Primary Renal
Disease Renal
Ablation

Aging, Diabetes
Melitus, Dietary
Factors

GLOMERULAR HYPERTENSION

ENDOTHELIAL INJURY
Release of vasoactive
factors
Vascular lipid deposition
Intracapillary thrombosis

MESANGIAL INJURY
Accumulation of macromolecules
Matrix production
 Cell proliferation

EPITHELIAL INJURY
Proteinuria
 Permeability to water

GLOMERULAR SCLEROSIS
Anderson S. Brenner. Q J Med 1989 ; 70 : 185-189.)

Proteinuria
Protein leakage
Protein load to
Proximal tubules

Interstitium
•Gene expression
for inflamation
•Transdifferentiation
to myofibloblast

Glomerular Hypertension

Ang II

TGF ß 1, etc

Fibrosis
Proliferation
Hypertension
Matrix synthesis

PROGRESSION of CKD

Eknoyan G, ASN Symp,Philadelphia,2002

Age-Standardized Rate of Cardiovascular
Events (per 100 person-yr)

CKD Predicts CVD

Estimated GFR (mL/min/1.73 m2)
Go, et al., 2004

Stage and
prevalence of CKD
in individuals older
than 20 years

Stage5

N=372,000
GFR <15*
N=400,000

Stage 4
GFR 15-29*
Stage 3
GFR 30-59*
N=7,600,00

Stage 2

GFR 60-89*
N=5,300,000

Stage 1
GFR>90*
N=5,900,000

*GFR measurement in mL/min/1.73 m2

7

ESRD
Hebert et aL: KI 2001 59:1211-26

.

 In

normal “healthy” individuals, the eGFR will fall
by up to 10 ml/min (ie 10%) per decade

 An

80 year old man will have an expected eGFR of
50-60 ml/min

RISK FACTORS FOR CKD
PROGRESSION
GENETIC

HYPERLIPIDEMIA GENDER

HYPERGLYCEMIA CIGARETTES

ANEMIA

RAAS ACTIVITY

HOMOCYSTEIN

HYPOKALEMIA

HYPERTENSION

SALT INTAKE

HYPERPHOSPHATEMIA

PROTEINURIA

PROTEIN INTAKE ENDOGENOUS
INSULIN EXCESS
Hebert et aL: KI 2001 59:1211-26

Cardiovascular disease in CKD
Damage to the heart
(Uraemic cardiomyopathy)

Damage to the arteries
(Uraemic arteriopathy)

Echocardiography
Starting Dialysis
Therapy

Kidney Int 1995

Comorbidities in CKD
100%

No CKD

80%

Stage 3 CKD
60%

Stage 4 CKD
Stage 5 CKD

40%

20%

0%
All cardiovascular
disease

Diabetes

Ischaemic heart
disease

Heart failure

P eripheral vascular
disease

Hypertension

GFR ( mL/min/1,73 m2)

“Original study performance using hematocrit
from Radtke et el, Blood 1979;54:877-884.

CARDIAC REMODELLING RESULTING FROM
ANEMIA AND HYPERTENSION
LVEDV :<90 ml/m2
CONCENTRIC
LVH

CKD

P
HY

An
e

N
IO
S
N
TE
R
E

DILATED LVH
WITH HEART
FAILURE

mia

Normal LVM :126 g/m2

ECCENTRIC
LVH
LVEDV :<90 ml/m2

LVH = left venticuler hypertrophy; LVM=LV mass; LVEDV=LV end diastolic volume

Lopez-Gomez et al.Kidney Int.1998;54:992-SEB; London et al. Adv Ren Replace
Ther. 1997;4:194-211. Casele et al.Ann Intern Medicine.1986;10:173-176

Anemia associated with increased risk of stroke
In CKD patients/

Eknoyan G, ASN Symp,Philadelphia,2002

Calcitriol Decline and iPTH Elevation
as CKD Progresses
CKD Stage 1
5.6 million

Stage 2
5.7 million

Stage 3
7.4 million

Stage 4
300,000

40
30
25
20

300
Low-Normal
Calcitriol

200

10
0

400
iPTH (pg/mL)

Calcitriol
1,25(OH)2D3 (pg/mL)

50

100
High-Normal 65
PTH
105

95

85

75

65

55

45

35

25

15

eGFR (mL/min/1.73 m2)
N = 150.
iPTH = intact PTH.
Adapted from Martinez et al. Nephrol Dial Transplant. 1996;11(suppl
3):22-28.
© 2005 The
Johns Hopkins University School of Medicine.

Systolic Blood Pressure and
Progression of CKD
AIPRD Study Group

5569 records with non-diabetic kidney disease
Meta-analysis of 11 RCTs of ACEIs

RR

Systolic BP (mmHg)
Jafar et al, Ann Intern Med 2003;139:244-252

Urine Protein Excretion and
Progression of CKD
AIPRD Study Group
4685 records with non-diabetic kidney disease
Meta-analysis of 11 RCTs of ACEIs
RR

Urine protein excretion (g/day)
Jafar et al, Ann Intern Med 2003;139:244-252

Synergistic effect of CKD,CHF and
Anemia as risk factors for Death
2 yr mortality (n~ 200,000 5% Medicare sample)
%

Collins, Adv studies in Med 2003

Eknoyan G, ASN Symp,Philadelphia,2002

Who are at risk?
 Those

who are hypertensive, diabetic, obese,

renal stone.
 Those with family history of:
hypertension, diabetes, and renal disease/
failure

Schoolwerth A, ANNA Meeting,2002

Infection / UTI
Dehydration
Acute on
Chronic

Obstructive
Electrolyte Disturb.
Severe Hypertension

CKD

STAGE 1

STAGE 2

Decrement
Renal
of recidual
insufficiency
renal function
risk

STAGE 3-4

STAGE 5

Renal failureESRD

risk

risk

Tx
Tx

Tx

Decisions in renal
replacement
 Pre-dialysis

care

 Active

-

treatment
Peritoneal dialysis (PD)
Haemodialysis (HD)
Transplantation

 Conservative

management.

(non-dialytic) care. Symptom

• Blood pressure and proteinuria control
• Correction of hyperglycaemia
• Dietary management
• Correction of calcium-phosphate
disorders
• Correction of hyperlipidaemia
• Correction of anemia and acidosis
• Cessation of smoking
• the importance of early referral to a
nephrologist

Decisions in renal
replacement
 Pre-dialysis

care
Treat: hypertension
hyperglycemia
hyperlipidemia
anemia

To target

Diet: Low Protein
Anti RAAS antihypertensives

Smoking and progression
rel. risk vs.
non-smokers

smokers,
no ACE inhibitors

10

0.001

smokers
treated with ACE inhibitors

1.3

N.S.

Orth, Kidn Intern (1998) 54: 926

Am J Kidney Dis 2002 39:376-82

Am J Kidney Dis 2002 39:376-82

ns

P=0.007

P=0.04
F

B

B

Control

F

Exercise

B F

Control

B

Exercise

F

Control

B

F

Exercise

B

B

F

Control

B

F

Exercise

Pengaruh regular mild aquatic exercise selama 3 bulan

F

Control

P=0.05

P=0.005
B

F

P=0.03

B

B

Exercise

ns

ns

F

B

Control

F

F

Exercise

Kidney International Vol 66 (2004), pp: 753-760

Kidney Int 2004 66: 753 - 60

Kidney Int 2004 66: 753 - 60

Kidney Int 2004 66: 753 - 60

Early Treatment Makes a Difference

MANAGEMENT
CKD

CONSERVATIVE
Diet :

Water + salt
Protein
Calori
Phosphate, K+

Risk-factors management
Symptomatic Medicament :

RRT

MANAGEMEN
T
CKD
RRT

Consernative
DIALYSIS

TRANSPLANT

Hemodialisa
Peritoneal
CAPD
IPD
Hemofiltration
Hemodiafiltration
Indication : vide AKI

Diabetes:
The Most Common Cause of ESRD
Primary Diagnosis for Patients Who Start Dialysis
Other

No. of dialysis patients (thousands)

10%

700

Glomerulonephritis
13%
Hypertension
27%

Diabetes
50.1%

600

No. of patients
Projection
95% CI

500
400
520,240

300
281,355

200
243,524

100
0

r2=99.8%
1984

1988

United States Renal Data System. Annual data report. 2000.

1992

1996

2000

2004

2008

Cardiovascular Mortality in the
General Population and in ESRD
by Dialysis
Annual mortalityTreated
(%)
100

Dialysis

10

General population

1
0.1

Male
Female

0.01

Black
White
25–34 35–44 45–54 55–64 65–74 75–84
Age (years)

85

MANAGEMENT
CKD

CONSERVATIVE

DIALYSIS

TRANSPLANT

Cadaver Kidne
Living Donor
Related
Un related

( Renal Replacement Therapy)
a. Dialysis
1. Peritoneal dialysis
(continuous ambulatory peritoneal
dialysis
= CAPD)
2. Hemodyalisis (HD)

b. RENAL TRANSPLANTATION
Donor

: Living (related, un-related)
Cadaver

Resipien Tissue Type - HLA-Match

Long term use of imuno-suppressive drugs
to cope with rejection

Messages to Take Home
 Kidney

Disease is a silent killer-(no signs or
symptoms until you loose >70% of your kidney
function,
 The risk of dying from a cardiovascular event, if
you’ve lost 50% or more of your kidney function,
is similar to that having had a heart attack.
 Proteinuria reduction needs to be a key part of
blood pressure management.

©2006. American College of Physicians. All Rights Reserved.